scholarly journals Microbial Community Heterogeneity Within Colorectal Neoplasia and its Correlation With Colorectal Carcinogenesis

2021 ◽  
Author(s):  
Weixin Liu ◽  
Xiang Zhang ◽  
Hongzhi Xu ◽  
Shengmian Li ◽  
Harry Cheuk-Hay Lau ◽  
...  
Keyword(s):  
Microbial Community ◽  
Colorectal Neoplasia ◽  
Colorectal Carcinogenesis ◽  
Community Heterogeneity

scholarly journals Circulating inflammation markers and colorectal adenoma risk

2019 ◽  
Vol 40 (6) ◽  
pp. 765-770 ◽  
Author(s):  
Wen-Yi Huang ◽  
Sonja I Berndt ◽  
Meredith S Shiels ◽  
Hormuzd A Katki ◽  
Anil K Chaturvedi ◽  
...  
Keyword(s):  
Colorectal Adenoma ◽  
Statistical Tests ◽  
Colorectal Neoplasia ◽  
Serum Levels ◽  
Colorectal Carcinogenesis ◽  
Inflammation Markers ◽  
Ovarian Cancer Screening ◽  
Cysteine Motif ◽  
Chemokine Ligand ◽  
Incident Cases

Abstract Inflammation is a driver of colorectal neoplasia; however, what particular inflammatory processes play a role in early carcinogenesis are unclear. We compared serum levels of 78 inflammation markers between 171 pathologically confirmed colorectal adenoma cases (including 48 incident cases) and 344 controls within the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. We used weighted multivariable logistic regression to compute odds ratio (OR) and 95% confidence interval (CI). We found 14 markers associated with risk of adenoma overall; three of these were also associated with incident adenoma: CC-chemokine cysteine motif chemokine ligand 20 (CCL20) [overall adenoma fourth versus first quartile: OR 4.8, 95% CI 2.0–12, Ptrend 0.0007; incident adenoma third versus first tertile: OR 4.6, 95% CI 1.0–22, Ptrend 0.03], growth-related gene oncogene products (GRO) [OR 3.8, 95% CI 1.6–9.3, Ptrend 0.006 and OR 3.6, 95% CI 1.1–12, Ptrend 0.04, respectively] and insulin [OR 2.9, 95% CI 0.8–10, Ptrend 0.05 and OR 7.8, 95% CI 1.3–46, Ptrend 0.03, respectively]. All statistical tests were two-sided. These results provide important new evidence implicating CCL20- and GRO-related pathways in early colorectal carcinogenesis and further support a role for insulin.

scholarly journals Mutation Profiling of Premalignant Colorectal Neoplasia

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Jakub Karczmarski ◽  
Krzysztof Goryca ◽  
Jacek Pachlewski ◽  
Michalina Dabrowska ◽  
Kazimiera Pysniak ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Colorectal Neoplasia ◽  
Copy Number Variant ◽  
Genetic Alterations ◽  
Colorectal Adenomas ◽  
Colorectal Carcinogenesis ◽  
High Grade Dysplasia ◽  
Low Grade ◽  
High Grade ◽  
Allelic Variants

Accumulation of allelic variants in genes that regulate cellular proliferation, differentiation, and apoptosis may result in expansion of the aberrant intestinal epithelium, generating adenomas. Herein, we compared the mutation profiles of conventional colorectal adenomas (CNADs) across stages of progression towards early carcinoma. DNA was isolated from 17 invasive adenocarcinomas (ACs) and 58 large CNADs, including 19 with low-grade dysplasia (LGD), 21 with LGD adjacent to areas of high-grade dysplasia and/or carcinoma (LGD-H), and 28 with high-grade dysplasia (HGD). Ion AmpliSeq Comprehensive Cancer Panel libraries were prepared and sequenced on the Ion Proton. We identified 956 unique allelic variants; of these, 499 were considered nonsynonymous variants. Eleven genes (APC, KRAS, SYNE1, NOTCH4, BLNK, FBXW7, GNAS, KMT2D, TAF1L, TCF7L2, and TP53) were mutated in at least 15% of all samples. Out of frequently mutated genes, TP53 and BCL2 had a consistent trend in mutation prevalence towards malignancy, while two other genes (HNF1A and FBXW7) exhibited the opposite trend. HGD adenomas had significantly higher mutation rates than LGD adenomas, while LGD-H adenomas exhibited mutation frequencies similar to those of LGD adenomas. A significant increase in copy number variant frequency was observed from LGD through HGD to malignant samples. The profiling of advanced CNADs demonstrated variations in mutation patterns among colorectal premalignancies. Only limited numbers of genes were repeatedly mutated while the majority were altered in single cases. Most genetic alterations in adenomas can be considered early contributors to colorectal carcinogenesis.

scholarly journals Role of S100 Proteins in Colorectal Carcinogenesis

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Paula Moravkova ◽  
Darina Kohoutova ◽  
Stanislav Rejchrt ◽  
Jiri Cyrany ◽  
Jan Bures
Keyword(s):  
Calcium Binding ◽  
Colorectal Neoplasia ◽  
Serum Levels ◽  
S100 Proteins ◽  
Colorectal Carcinogenesis ◽  
Invasion And Migration ◽  
Common Cancer ◽  
The Family ◽  
And Migration

The family of S100 proteins represents 25 relatively small (9–13 kD) calcium binding proteins. These proteins possess a broad spectrum of important intracellular and extracellular functions. Colorectal cancer is the third most common cancer in men (after lung and prostate cancer) and the second most frequent cancer in women (after breast cancer) worldwide. S100 proteins are involved in the colorectal carcinogenesis through different mechanisms: they enable proliferation, invasion, and migration of the tumour cells; furthermore, S100 proteins increase angiogenesis and activate NF-κβsignaling pathway, which plays a key role in the molecular pathogenesis especially of colitis-associated carcinoma. The expression of S100 proteins in the cancerous tissue and serum levels of S100 proteins might be used as a precise diagnostic and prognostic marker in patients with suspected or already diagnosed colorectal neoplasia. Possibly, in the future, S100 proteins will be a therapeutic target for tailored anticancer therapy.

scholarly journals Comparing microbial community heterogeneity in soil under organic and conventional agricultural system cultivated with olive and peach trees in three fields differ with age at Al-Jouf Saudi Arabia

2020 ◽  
Vol 7 (3) ◽  
pp. 283-290
Author(s):  
Ahmad Yassin Majjami ◽  
Abdullah Saad Al-Modaihsh ◽  
Fahad Nasser Al-Barakah ◽  
Mohamed Hamza El-Saeid ◽  
Samir Gamil Al-Solimani ◽  
...  
Keyword(s):  
Saudi Arabia ◽  
Microbial Community ◽  
Agricultural System ◽  
Community Heterogeneity ◽  
Peach Trees

scholarly journals Possible predisposition for colorectal carcinogenesis due to altered gene expressions in normal appearing mucosa from patients with colorectal neoplasia

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Christian Hunnicke Petersen ◽  
Badar Mahmood ◽  
Christoffer Badsted ◽  
Tina Dahlby ◽  
Hanne Borger Rasmussen ◽  
...  
Keyword(s):  
Colorectal Neoplasia ◽  
Colorectal Carcinogenesis ◽  
Gene Expressions ◽  
Altered Gene

scholarly journals Updates on Translational Research on Prevention of Polyps and Colorectal Cancer

2018 ◽  
Vol 31 (03) ◽  
pp. 153-160 ◽  
Author(s):  
Elena Stoffel
Keyword(s):  
Colorectal Cancer ◽  
Early Detection ◽  
Secondary Prevention ◽  
Randomized Clinical Trials ◽  
Colorectal Neoplasia ◽  
The United States ◽  
Colorectal Carcinogenesis ◽  
Dietary Interventions ◽  
Asymptomatic Individuals ◽  
Pharmacologic Agents

AbstractMorbidity and mortality from colorectal cancer (CRC) can be effectively reduced through early detection and prevention. To date, strategies for managing CRC risk have focused primarily on secondary prevention, through screening asymptomatic individuals for colorectal neoplasia. In the United States, implementation of screening among individuals age ≥50 has led to not only decreased CRC-related mortality but also reduced CRC incidence through colonoscopic removal of precancerous polyps. In contrast to screening's endpoint of early detection, the goal of primary prevention of CRC is to arrest and/or reverse colorectal carcinogenesis. Observational studies and randomized clinical trials continue to examine effects of specific pharmacologic agents (chemoprevention) and dietary interventions on development of advanced colorectal neoplasia. This review will present an overview of strategies for primary and secondary prevention of CRC, including endoscopic, pharmacologic, and dietary interventions.

scholarly journals The Role of the Gut Microbiota in Colorectal Cancer Causation

2019 ◽  
Vol 20 (21) ◽  
pp. 5295 ◽  
Author(s):  
Alhinai ◽  
Walton ◽  
Commane
Keyword(s):  
Colorectal Cancer ◽  
Microbial Community ◽  
Gut Microbiota ◽  
Fusobacterium Nucleatum ◽  
Colorectal Carcinogenesis ◽  
Cell Behaviour ◽  
Streptococcus Gallolyticus ◽  
Chemically Induced ◽  
Carcinogenic Process

Here, we reviewed emerging evidence on the role of the microbial community in colorectal carcinogenesis. A healthy gut microbiota promotes intestinal homeostasis and can exert anti-cancer effects; however, this microbiota also produces a variety of metabolites that are genotoxic and which can negatively influence epithelial cell behaviour. Disturbances in the normal microbial balance, known as dysbiosis, are frequently observed in colorectal cancer (CRC) patients. Microbial species linked to CRC include certain strains of Bacteroides fragilis, Escherichia coli, Streptococcus gallolyticus, Enterococcus faecalis and Fusobacterium nucleatum, amongst others. Whether these microbes are merely passive dwellers exploiting the tumour environment, or rather, active protagonists in the carcinogenic process is the subject of much research. The incidence of chemically-induced tumours in mice models varies, depending upon the presence or absence of these microorganisms, thus strongly suggesting influences on disease causation. Putative mechanistic explanations differentially link these strains to DNA damage, inflammation, aberrant cell behaviour and immune suppression. In the future, modulating the composition and metabolic activity of this microbial community may have a role in prevention and therapy.

scholarly journals Braf mutation induces rapid neoplastic transformation in the aged and aberrantly methylated intestinal epithelium

Gut ◽  
2021 ◽  
pp. gutjnl-2020-322166
Author(s):  
Lochlan Fennell ◽  
Alexandra Kane ◽  
Cheng Liu ◽  
Diane McKeone ◽  
Gunter Hartel ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Colorectal Neoplasia ◽  
Young Patients ◽  
Neoplastic Transformation ◽  
The Elderly ◽  
Colorectal Carcinogenesis ◽  
Neoplastic Progression ◽  
Molecular Alterations ◽  
Serrated Lesions ◽  
Aberrant Dna Methylation

ObjectiveSessile serrated lesions (SSLs) are common across the age spectrum, but the BRAF mutant cancers arising occur predominantly in the elderly. Aberrant DNA methylation is uncommon in SSL from young patients. Here, we interrogate the role of ageing and DNA methylation in SSL initiation and progression.DesignWe used an inducible model of Braf mutation to direct recombination of the oncogenic Braf V637E allele to the murine intestine. BRAF mutation was activated after periods of ageing, and tissue was assessed for histological, DNA methylation and gene expression changes thereafter. We also investigated DNA methylation alterations in human SSLs.ResultsInducing Braf mutation in aged mice was associated with a 10-fold relative risk of serrated lesions compared with young mice. There were extensive differences in age-associated DNA methylation between animals induced at 9 months versus wean, with relatively little differential Braf-specific methylation. DNA methylation at WNT pathway genes scales with age and Braf mutation accelerated age-associated DNA methylation. In human SSLs, increased epigenetic age was associated with high-risk serrated colorectal neoplasia.ConclusionsSSLs arising in the aged intestine are at a significantly higher risk of spontaneous neoplastic progression. These findings provide support for a new conceptual model for serrated colorectal carcinogenesis, whereby risk of Braf-induced neoplastic transformation is dependent on age and may be related to age-associated molecular alterations that accumulate in the ageing intestine, including DNA methylation. This may have implications for surveillance and chemopreventive strategies targeting the epigenome.

A peek in the micro-sized world: a review of design principles, engineering tools, and applications of engineered microbial community

2020 ◽  
Vol 48 (2) ◽  
pp. 399-409
Author(s):  
Baizhen Gao ◽  
Rushant Sabnis ◽  
Tommaso Costantini ◽  
Robert Jinkerson ◽  
Qing Sun
Keyword(s):  
Microbial Community ◽  
Microbial Communities ◽  
Environmental Remediation ◽  
Real Life ◽  
Design Principles ◽  
Microbial Interactions ◽  
Potential Applications ◽  
New Gene ◽  
Global Biogeochemical Cycles ◽  
Synthetic Microbial Communities

Microbial communities drive diverse processes that impact nearly everything on this planet, from global biogeochemical cycles to human health. Harnessing the power of these microorganisms could provide solutions to many of the challenges that face society. However, naturally occurring microbial communities are not optimized for anthropogenic use. An emerging area of research is focusing on engineering synthetic microbial communities to carry out predefined functions. Microbial community engineers are applying design principles like top-down and bottom-up approaches to create synthetic microbial communities having a myriad of real-life applications in health care, disease prevention, and environmental remediation. Multiple genetic engineering tools and delivery approaches can be used to ‘knock-in' new gene functions into microbial communities. A systematic study of the microbial interactions, community assembling principles, and engineering tools are necessary for us to understand the microbial community and to better utilize them. Continued analysis and effort are required to further the current and potential applications of synthetic microbial communities.

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